Biology subjects

Justman, Q.

Publications and source records attributed to Justman, Q..

3 recordsLinked to original sources

bioRxiv2026

Division of labor during bacterial warfare

Division of labor is commonly associated with cooperative behavior, yet one of its most extreme forms occurs during bacterial warfare, where a subset of cells undergoes suicidal lysis to release toxins. Why bacteria divide labor among a few cells rather than producing toxin uniformly remains unknown. Here, we combine timelapse microscopy and simulations, to understand the division of labor during bacterial warfare using bacteriocin (colicin) production by the gut bacterium Escherichia coli as a model system. At the single-cell level, we find that lytic toxin production is a tightly regulated event: only cells that commit to lysis produce significant toxin and then lysis only occurs once a large amount of toxin has been made. This high threshold ensures each sacrifice delivers a large dose, which is released in a rapid burst from a lysing cell. While such burst-like release appears to provide no advantage over uniform labor in well-mixed conditions, we show it becomes extremely effective in spatially structured populations where the rapid release of toxin by one cell can generate lethal concentrations locally and eliminate competitors. Finally, we explain why the lysing fraction remains so small. While an increase in the producing cells increases toxin levels, it also increases the probability of local patch extinctions. The division of labor during bacterial warfare, therefore, enables powerful localized killing while safeguarding the population from self-destruction.

microbiology↗

bioRxiv2026

Inherited flagellar structures coordinate the onset of swimming among related E. coli cells

Bacteria commit to costly behaviors before they can benefit from them. In Escherichia coli, flagellar synthesis is expensive, yet the genes are expressed in stochastic pulses and only a small minority of pulses result in motility. Despite this noise, we find that lineage-related cells begin swimming at similar times, in groups of two to eight cells. Rare, high-amplitude pulses commit a single cell within one generation, but more commonly, pulses rise slowly and fail to trigger swimming before division. Rather than decaying, their output accumulates as cells inherit hook-basal bodies (HBBs) and continue to build new ones. This structural inheritance acts as a physical integrator, summing ongoing transcriptional activity across generations, so that an incomplete flagellar cascade is carried forward at division rather than lost. HBB accumulation sets when cells swim, and the anti-sigma factor FlgM sets how sharply. By holding late flagellar genes off until several HBBs have accumulated, FlgM makes motility depend steeply on early flagellar gene expression, so that relatives inheriting similar sets of HBBs become motile together. Without FlgM, this sharp dependence is largely lost, and activations of the full cascade do not reliably produce swimming. Together, our results show how the accumulation of a molecular machine integrates fluctuations, and how a checkpoint on its assembly sharpens them into a decision, setting both the speed and heritability of a behavioral trait.

systems biology↗

bioRxiv2023

A long-acting prolactin to combat lactation insufficiency

Human infants are born to breastfeed. While 50% of lactating persons struggle to make enough milk, there are no governmentally-approved drugs to enhance lactation1. Here, we engineer a variant of the naturally-occurring driver of lactation, the hormone Prolactin, to increase its serum half-life and produce a viable drug candidate. Our engineered variant, Prolactin-eXtra Long-acting (Prolactin-XL), is comprised of endogenously active human prolactin fused to an engineered human IgG Fc domain designed to overcome the unique drug development challenges specific to the lactating person-infant dyad. Our Prolactin-XL has a serum half-life of 70.9h in mice, 2,625-fold longer than endogenously active prolactin alone (70.9h v. 0.027h). We demonstrate that Prolactin-XL increases milk production and restores growth of pups fed by dams with pharmacologically-ablated lactation. We show that Prolactin-XL-enhanced lactation is accompanied by reversible, lactocyte-driven changes in mammary gland morphology. This work establishes long-acting prolactins as a potentially powerful pharmacologic means to combat insufficient lactation.

synthetic biology↗